Targeting beta-adrenergic signalling to improve muscle regeneration in muscular dystrophy

靶向β-肾上腺素能信号传导以改善肌营养不良症的肌肉再生

• 批准号: nhmrc : 509313
• 负责人: A/Pr Paul Gregorevic
• 金额: $ 31.55万
• 依托单位: The University of Melbourne
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2008
• 资助国家: 澳大利亚
• 起止时间: 2008-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/targeting-beta-adrenergic-muscular-dystrophy/78476
• 关键词: Targeting; beta; adrenergic; signalling; improve

Duchenne muscular dystrophy (DMD) is the most common and severe form of muscular dystrophy, caused by a lack of a protein called dystrophin. Dystrophic muscles are fragile, prone to injury, and have a compromised ability to regenerate after damage. Modulating pathways regulating beta-adrenergic signalling has potential to attenuate the dystrophic pathology and to delay the onset or slow the progression of the muscle wasting and weakness in muscular dystrophy.

杜氏肌营养不良症 (DMD) 是最常见和最严重的肌营养不良症，由缺乏一种称为肌营养不良蛋白的蛋白质引起。营养不良的肌肉很脆弱，容易受伤，并且损伤后再生能力受损。调节β-肾上腺素能信号传导途径有可能减轻肌营养不良症的病理学并延迟肌营养不良症中肌肉萎缩和无力的发作或减缓其进展。